Severe organophosphate intoxication without classic cholinergic signs: A case report and updated literature review

Abstract

Organophosphate compounds such as dichlorvos, a widely used pesticide, account for a substantial proportion of acute poisonings globally. These agents irreversibly inhibit acetylcholinesterase, leading to cholinergic overstimulation. A subgroup of these compounds, alkyl phosphates—originally developed as nerve agents such as tabun, sarin and soman—has been increasingly implicated in intentional ingestions. Diagnosis can be challenging, particularly in the absence of classic cholinergic features such as bradycardia, bronchorrhea and miosis. We present a case of a male patient in his early 20s who was admitted to the intensive care unit with impaired consciousness, respiratory failure, tachycardia and severe metabolic acidosis following ingestion of unidentified substances. Imaging revealed chemical gastritis and aspiration pneumonia. A profoundly reduced serum cholinesterase level prompted empiric initiation of obidoxime therapy. Admission toxicology was positive for amphetamines, plausibly explaining the patient's atypical tachycardia and attenuation of classical cholinergic signs. The patient recovered following intensive supportive care and later confirmed ingestion of dichlorvos in a suicide attempt. This review discusses the clinical presentation, diagnostic challenges and current evidence-based management of alkyl phosphate intoxication. Particular emphasis is placed on the utility of serum cholinesterase measurement, the role of oximes such as obidoxime, and adjunctive interventions including seizure control, and ventilatory support. Clinicians should be aware that severe organophosphate poisoning may occur even in the absence of classical cholinergic signs, requiring a high index of suspicion and timely antidotal therapy.

Introduction

Suicidal ideation, in both its passive and active forms, constitutes a significant public health issue with the potential to advance to overt suicidal behaviour. ¹ Pesticide self-poisoning remains a leading method of suicide worldwide, particularly in low- and middle-income countries, with organophosphate insecticides frequently implicated. ² Recent estimates suggest that pesticides account for ∼14%–20% of global suicides, with a disproportionately high burden in South Asia, South-East Asia and China.^3–5 In Germany, intensive care physicians treat about 200 patients annually after suicidal ingestion of these substances, approximately 30% of whom do not survive. ⁶ Organophosphates (OPs) are a diverse class of organophosphorus compounds, typically esters or amides of phosphoric or phosphorothioic acids. After exposure, OPs inhibit acetylcholinesterase (AChE) by phosphorylating its active site; unless promptly reactivated (e.g. with oximes), the inhibited enzyme ‘ages’ and becomes irreversibly inactivated. The resulting accumulation of acetylcholine produces a cholinergic toxidrome with nicotinic, muscarinic and central nervous system (CNS) features.

It should be taken into account that the direct precursor of acetylcholine is choline, an essential micronutrient required for cellular and systemic homeostasis. Moreover, choline metabolism contributes to a wide range of developmental and physiological processes and plays a key regulatory role, particularly in the brain, liver, kidneys, lungs and the immune system.^7,8

This case report describes an adult man from Nigeria who attempted suicide using an alkyl phosphate compound yet presented without the typical cholinergic signs of such intoxication. To contextualize this case and assess the current evidence on diagnosis and treatment of alkyl phosphate poisoning, we conducted a systematic literature review of publications on Dichlorvos and related compounds. The aim was to summarize relevant pathophysiological mechanisms, clinical features and therapeutic strategies based on the existing scientific literature.

Case report

In mid-2024, a male patient in his early 20s was admitted to the intensive care unit (ICU) of Klinikum Stuttgart (Stuttgart, Germany) through the emergency department after being found unconscious at the airport. Given the circumstances, a suicide attempt involving an unknown solvent at an unspecified time was suspected. Written informed consent for publication of the case details and images was obtained from the patient. The patient had a history of hospitalizations due to amphetamine intoxication. Upon admission, neurological examination revealed a Glasgow Coma Scale (GCS) of 13/15. ⁹ Cranial imaging was unremarkable. He was breathing spontaneously but presented with hypertension, tachycardia and hypothermia. Protective reflexes were preserved (Table 1). A detailed medical history could not be obtained due to a language barrier and the patient's reduced level of consciousness. However, he repeatedly expressed clearly articulated suicidal thoughts. Initially, no reliable information regarding substance ingestion could be obtained.

Table 1.

Vital parameters of the patient during the first 6 h of inpatient stay (prior to intubation).

Time (h)	Blood pressure (mmHg)	Heart rate (bpm)	Temperature (°C)	Oxygen saturation (%)	Respiratory rate (bpm)
1	147/77	106	34.0	96	24
2	168/88	107	35.3	97	19
3	162/72	110	—	97	10
4	164/74	104	—	98	12
5	161/73	98	—	95	31
6	162/78	145	—	90	39

Blood gas analysis revealed metabolic acidosis with hypokalemia (2.5 mmol/L) and hyperglycaemia (226 mg/dL) (Table 2). A strong solvent-like odour was detected on the patient's breath, in the blood and in the aspirated gastric contents, which also contained yellowish secretions. Toxicological urine screening was positive for MDMA, amphetamines, ecstasy and cannabis. Given the metabolic acidosis with an elevated anion gap, the presence of a solvent odour, and suspected intoxication with acetone or other alcohols, blood and gastric samples were sent to Saarland University in Homburg for specialized analysis. However, the results were inconclusive.

Table 2.

Laboratory parameters of the patient during intensive care unit stay.

Parameter	Day 1	Day 2	Day 3	Day 4	Day 5	Day 6	Day 7
pH (7.35–7.45)	7.22	7.32	7.43	7.46	7.47	7.46	7.4
HCO3- (22–26 mmol/L)	13.2	19.6	22.3	25.4	26.1	24.4	24
Lactate (0.5–2.2 mmol/L)	3.5	0.9	1.3	0.8	0.6	0.7	2.8
Blood glucose (70–100 mg/dL)	226	130	113	95	119	116	126
Potassium (3.4–4.5 mmol/L)	2.5	3.8	4.2	3.7	3.9	4	3.5
Urea (15–41 mg/dL)	24	34	39	21	11	13	17
Creatinine (0.5–0.9 mg/dL)	1.0	1.5	1.0	1.0	0.8	0.9	1.0
Total bilirubin (<1.3 mg/dL)	—	1.0	1.1	1.0	—	0.7	0.4
AST (<50 U/L)	78	51	91	74	71	78	62
ALT (<50 U/L)	24	37	31	30	33	58	72
GGT (<60 U/L)	156	141	105	80	145	210	192
BChE (CHE) (7–19 kU/L)	<1.5	<1.5	<1.5	2.6	3.7	4.5	4.8

Note: BChE (ChE) = plasma/serum butyrylcholinesterase activity, measured by photometric routine assay.

Clinically, the patient appeared to be in normal nutritional status (BMI 21.8) but exhibited a reduced general condition. His pupils were miotic, isocoric and reactive to light. Auscultation revealed expiratory rales. Point-of-care ultrasonography showed a distended stomach despite the presence of a nasogastric tube and hypovolemic circulation with a collapsed inferior vena cava.

As the patient's consciousness and respiratory status deteriorated, endotracheal intubation became necessary due to hypersecretion, bronchospasm and worsening metabolic acidosis. During pressure-controlled ventilation with a positive end-expiratory pressure (PEEP) of 10 mmHg and an inspiratory oxygen fraction (FiO₂) of 25%, the patient maintained a peripheral oxygen saturation of 100%. A Shaldon catheter was inserted in case emergency dialysis became necessary. However, multiple doses of 8.4% sodium bicarbonate quickly normalized the pH, and dialysis was not required.

CT imaging revealed gastric wall thickening with interstitial fluid accumulation and persistent intragastric contents, despite nasogastric drainage. Upper endoscopy showed whitish mucosa, indicative of localized chemical injury, but no active bleeding. A proton pump inhibitor (PPI) was started at double the standard dose.

Due to CT-confirmed aspiration pneumonia in the left lower lobe, a 5-day course of ampicillin/sulbactam was initiated. Initial bronchoscopy revealed whitish foam; follow-up the next day showed opaque plaques and purulent secretions, confirming aspiration pneumonia.

Given the combination of hypertension, mild hyperglycaemia, respiratory deterioration with hypersalivation and pseudopulmonary edema, alkyl phosphate poisoning was suspected. Although bradycardia represents the characteristic cardiovascular manifestation of organophosphate poisoning, this patient exhibited tachycardia. However, butyrylcholinesterase (BChE) activity was severely reduced, falling below measurable limits (Table 2), thereby reinforcing the suspicion of alkyl phosphate intoxication. Analgesic sedation was maintained with remifentanil and propofol, complemented by midazolam at a continuous infusion rate of 0.2 mg/kg/h to provide neuroprotective effects. The cholinergic symptoms were treated from the first day of therapy with bolus administrations of atropine at doses of 2 mg, doubling every 5 min, resulting in a total of 15 mg administered. This was followed by a continuous infusion at a rate of 0.05 mg/kg/h until the sixth day of treatment. Additionally, a specific oxime therapy with obidoxime was initiated to reactivate the acetylcholinesterase inhibited by the organophosphates (Figure 1). The patient received a 250 mg IV bolus, followed by a continuous infusion of 750 mg over 24 h for five consecutive days. Serum BChE activity steadily increased during obidoxime therapy, most recently reaching 4.8 kU/L (Table 2).

Figure 1.

Clinical course (days 1–7) during intensive care. Selected clinical findings, treatments and laboratory trends. Reference ranges are shown in brackets. Atropine: continuous infusion 0.05 mg/kg/h; obidoxime: 750 mg over 24 h; benzodiazepine: diazepam 10 mg initially every 2 h, followed by a stepwise dose reduction. BChE: plasma/serum butyrylcholinesterase activity; ChE: routinely measured BChE; Ery-AChE: erythrocyte acetylcholinesterase activity. ¹Routine photometric assay (clinical laboratory). ²Measured by Ellman assay (toxicology laboratory).

Toxicological analysis at the Bundeswehr Central Institute in Munich did not detect any free organophosphate in the blood. However, erythrocyte acetylcholinesterase (AChE) activity was completely inhibited and no longer reactivatable, indicating irreversible binding by an organophosphate; therefore, obidoxime therapy was discontinued on day 6 (Figure 1).

Following clinical stabilization, the patient was successfully extubated on the second day of obidoxime therapy. To maintain the neuroprotective effect, benzodiazepine therapy was continued after extubation with diazepam substituted for midazolam. On the first day after extubation, the patient received diazepam 10 mg every 2 h. The clinical course was monitored using the CIWA-Ar scale, ¹⁰ and the dose was gradually tapered over the following days. Although the CIWA-Ar scale is primarily intended for evaluating alcohol withdrawal, it was used in this context because the patient had a documented alcohol use disorder and concomitant alcohol intoxication during the prior hospital stay. Although still confused and agitated, his overall condition improved rapidly.

After completion of intensive care treatment, the patient was transferred to a psychiatric facility for further management. He later reported intentional ingestion of Dichlorvos, an insecticide marketed in Nigeria under the trade name Sniper. All patient identifiers have been removed from images and data tables to protect patient confidentiality. We have de-identified all patient details to protect confidentiality. The reporting of this case conforms to the CARE guidelines. ¹¹

Discussion

To identify relevant scientific studies on Dichlorvos and alkyl phosphate poisoning, a systematic literature search was conducted in the MEDLINE database (via PubMed). The search was limited to publications between 1980 and 2024. Specific search terms included ‘suicide’, ‘Dichlorvos’, ‘organophosphate’, ‘organophosphate poisoning’, ‘intoxication’, ‘cellular metabolism of Dichlorvos’, ‘symptomatology and differential diagnosis of organophosphate intoxication’ and ‘therapy’.

Toxicology

Alkyl phosphates are widely used as insecticides and exert their toxicological effects primarily through the irreversible inhibition of acetylcholinesterase (AChE). Dichlorvos (2,2-dichlorovinyl dimethyl phosphate), the agent involved in our case, readily penetrates biological membranes and accumulates in the cytoplasm owing to its solubility in both water and lipids. The reported lethal oral dose of Dichlorvos in humans is approximately 70 mg/kg. ⁶

Chemically, alkyl phosphates are composed of phosphoric acid (H₃PO₄) and a corresponding alcohol. They can be absorbed via the lungs, gastrointestinal tract and skin. Most exhibits pronounced lipophilic properties and a high volume of distribution, leading to accumulation particularly in adipose tissue, the kidneys and the liver. This extensive distribution partially protects them from metabolism. The degree of lipophilicity, as well as the patient's fat mass, can significantly influence clinical outcomes following poisoning. A 2014 Korean study demonstrated that patients with a body mass index (BMI) above 25 experienced prolonged ventilation times, longer stays in the intensive care unit and overall extended hospitalization. ¹²

A defining feature of alkyl phosphate insecticides is their ability to inhibit carboxylester hydrolases, particularly acetylcholinesterase (AChE). These compounds phosphorylate the serine hydroxyl group of the enzyme, thereby inactivating AChE. As AChE is essential for the breakdown of acetylcholine, its inhibition leads to synaptic accumulation of acetylcholine and subsequent overstimulation of nicotinic and muscarinic receptors.^13,14 Restoration of enzymatic activity requires de novo synthesis of AChE in the liver. ¹⁵ Moreover, pseudocholinesterase (PsCE, also referred to as plasma cholinesterase or butyrylcholinesterase [BChE]) and neuropathy target esterase (NTE) are also inhibited.^16,17 BChE is widely distributed in plasma and various organs, including the liver, heart, pancreas and brain. BChE is a serine hydrolase that catalyzes the hydrolysis of a broad range of endogenous esters and xenobiotics. Beyond its classical enzymatic activity, recent studies have clarified its involvement in lipid metabolism and metabolic regulation. Although it is not as essential as acetylcholinesterase for neurotransmission, BChE serves as an important bioscavenger for organophosphates and related toxins. ¹⁸

An additional toxicological risk arises from the redistribution of organophosphates from adipose tissue back into the circulation or via gastrointestinal reabsorption. ¹⁹ Following binding to AChE, organophosphates undergo cleavage and form a stable but reversible phosphorylated complex that inactivates the enzyme. Although spontaneous reactivation is possible, this process occurs considerably more slowly and may require hours to days for functional recovery. ¹⁹

While some organophosphates are metabolized into more potent AChE inhibitors, dichlorvos is rapidly degraded, particularly in the skin, respiratory tract, gastrointestinal tract, heart and brain, via esterase-mediated hydrolysis into dimethyl phosphate and dichloroacetaldehyde. These metabolites are less toxic and exhibit lower affinity for AChE. Dimethyl phosphate is predominantly excreted, whereas dichloroacetaldehyde undergoes further metabolism. ²⁰ In addition to neurotoxicity, organophosphates such as dichlorvos are also associated with direct hepatotoxicity and nephrotoxicity.

Symptoms and diagnosis

The identification of organophosphate poisoning is a complex and time-consuming process, in which clinical and laboratory differential diagnoses are particularly important. Alkyl phosphates can induce a broad spectrum of toxic effects on the central and peripheral nervous systems, the cardiovascular system and the respiratory system. Classically, three symptom clusters are observed: (a) muscarinic cholinergic symptoms (SLUDGE syndrome), (b) nicotinic cholinergic symptoms and (c) central nervous system symptoms (Table 3). ²¹

Table 3.

Symptoms of acute alkyl phosphate intoxication.

Muscarinic cholinergic symptoms (SLUDGE syndrome)	Nicotinic cholinergic symptoms	Central nervous system symptoms
Miosis Visual accommodation disorders Increased secretion from lacrimal, sweat, salivary and tracheobronchial mucus glands Stimulation of the smooth muscle tissue in: - the gastrointestinal tract (vomiting, diarrhoea, colic) - the urogenital system (e.g. urinary urgency) Vasodilation Bradycardia Cardiac arrhythmias	Muscle twitching of the eyelids and tongue Occasional hypertension and hyperglycaemia Generalized fasciculations Tremors Muscle spasms Muscle weakness Respiratory muscle paralysis	Agitation Confusion Headache Unsteady gait Ataxia Dysarthria Vertical and horizontal nystagmus Tonic-clonic seizures Altered level of consciousness up to coma Respiratory and circulatory depression.

The range of findings observed in our patient due to overstimulation of muscarinic and nicotinic receptors corresponded to those reported in the literature: miosis, hypersalivation, diaphoresis, dyspnoea, hypertension, hyperglycaemia, and weakness of the limb and respiratory muscles. However, in contrast to typical cases described by Thiermann et al. ²² and Eddleston et al., ¹⁶ our patient presented with marked tachycardia rather than bradycardia, illustrating a rare cardiovascular response in acute dichlorvos intoxication.

Early symptoms typically arise from acetylcholinesterase inhibition, leading to acetylcholine accumulation and overstimulation of muscarinic receptors within 1–2 h of exposure. Delayed symptoms may occur 12–96 h post-exposure and result from continued acetylcholine accumulation at neuromuscular junctions. These manifest as nicotinic effects, such as weakness of the limb and respiratory muscles, as observed in our patient. Additionally, organophosphates promote glycogenolysis in the liver and lipolysis in adipose tissue. ²¹

Miosis, also observed in our patient, is one of the most common symptoms of alkyl phosphate poisoning, occurring in 44%–83% of cases.^23,24 Miosis and a sensation of chest tightness may result from pronounced local anti-AChE activity. ¹³ A garlic-like odour in the breath or vomitus is another characteristic feature, which was also noted in our patient.

Bradycardia represents the most common classical muscarinic cardiovascular manifestation of organophosphate poisoning. In the present case, however, tachycardia was observed—a finding which, despite its seemingly atypical presentation, is not unusual in the clinical context of organophosphate intoxication, as tachycardia may reflect an expected nicotinic or sympathetic effect of organophosphates. ²⁵

In addition, the pronounced tachycardia in this case can plausibly be explained by the simultaneous use of MDMA, ecstasy (street preparations containing MDMA in combination with other substances), amphetamines and cannabis. These substances exert predominantly sympathomimetic effects that counteract cholinergically mediated bradyarrhythmia and further potentiate the nicotinic–sympathetic effect with consequent tachycardia. ²⁶

Particularly lipophilic organophosphates with high CNS penetration and prolonged persistence may induce marked autonomic dysregulation, manifesting as alternating tachyarrhythmias and bradyarrhythmias. This finding reflects the complex interplay of central cholinergic overstimulation, impaired baroreflex regulation and autonomic ganglion activation. ²⁷ Finally, it should be emphasized that the presence of tachycardia does not constitute a contraindication to atropine therapy, as the indication is determined primarily by the presence of clinically relevant muscarinic symptoms. ²⁸

Clinical manifestations can include ventricular arrhythmias and Torsades de Pointes, potentially progressing to ventricular fibrillation or asystole. Common cardiac rhythm disturbances include atrioventricular (AV) block and QTc prolongation. ST-segment changes may also occur, and troponin monitoring is therefore recommended in severe cases. ²⁹ In our patient, no troponin elevation was detected. A case report from India described refractory asystole 12 days after organophosphate exposure. ³⁰

Toxicological confirmation of organophosphate poisoning relies on measuring erythrocyte acetylcholinesterase (Ery-AChE) and plasma/serum butyrylcholinesterase (BChE, pseudocholinesterase). Depressed activity supports exposure ³¹ ; Ery-AChE reflects synaptic AChE inhibition, whereas BChE is more sensitive but less specific. In our case, targeted toxicology sent on day 1 to an external laboratory was unsuccessful (no reportable result). A repeat analysis on day 6 at the Bundeswehr Central Institute, Munich yielded Ery-AChE 34.2 mU/µmol Hb—∼6% of typical reference values—indicating severe inhibition, and plasma BChE 1.2 U/mL (≈1.2 kU/L), also markedly depressed. Routine ‘ChE’ (i.e. BChE activity) measured photometrically in heparinized plasma was <1.5 kU/L on days 1–3 (reference 7.0–19.0 kU/L), rising to 4.5 kU/L by day 6 but remaining subnormal (Figure 1). Despite continuous obidoxime, meaningful Ery-AChE reactivation had not occurred by day 6; given the rapid ‘ageing’ of dichlorvos-inhibited AChE, ²¹ the therapeutic window for oxime efficacy is narrow.

Chromatographic techniques, particularly gas chromatography (GC) and liquid chromatography (LC), are routinely employed for the analysis of organophosphates and their metabolites in biological and environmental samples. ³² These methods allow precise separation and quantification of these compounds. Typically, toxin levels reach their peak between days 4 and 6, due to enterohepatic recirculation. In our case, no residual toxin was detected in plasma during follow-up testing on day 6.

In human biomonitoring, urinary dialkyl phosphates (DAPs) are primarily measured as markers of exposure. Most organophosphate pesticides are metabolized into one or more of the following metabolites: dimethyl phosphate, diethyl phosphate, dimethyl thiophosphate, diethyl thiophosphate, dimethyl dithiophosphate and diethyl dithiophosphate. These metabolites reflect exposure but are non-specific for the parent compound.^21,32

Laboratory indicators of liver injury, particularly elevated aminotransferases and gamma-glutamyltransferase, were detected in our case prior to the initiation of obidoxime therapy. Hepatic injury has been attributed to obidoxime treatment in the literature.^33,34

Management

Treatment of dichlorvos poisoning involves decontamination, specific antidotes and supportive measures. In cases of severe poisoning, early intubation is indicated to secure the airway and prevent aspiration. Following oral ingestion, gastric lavage should be performed promptly, followed by activated charcoal to limit absorption.^21,35

The main antidotes are atropine and oximes, particularly obidoxime (Toxogonin) (Table 4).

Table 4.

Therapeutic regimen for the management of organophosphate poisoning.

Drug	Dosage (adults)	Special considerations/therapeutic goal
Atropine	❖ Initial: 2–5 mg i.v. ❖ Repeat every 3–5 min, doubling each dose until effect (often >50 mg required) ❖ Continuous infusion: 0.02–0.08 mg/kg/h	Selective for muscarinic symptoms (bronchorrhoea, bradycardia); titrate to achieve clear airways, heart rate >80 bpm and stable oxygenation.
Obidoxime (oxime)	❖ Initial: 250 mg i.v. administered slowly over 5–10 min; ❖ Subsequently: 750 mg/24 h as continuous infusion, or 250 mg i.v. every 6–12 h	Reactivates AChE; alternative to pralidoxime; preferred in some European guidelines; administer early; monitor neuromuscular recovery and adverse effects
Pralidoxime (oxime)	❖ Initial: 30 mg/kg i.v. (≈1–2 g) over 20–30 min; ❖ Subsequently: 8–10 mg/kg/h (≈500 mg/h) as continuous infusion, or 0.5–1 g i.v. every 4–6 h	Reactivates AChE before ‘aging’; effective for muscle paralysis, fasciculations, respiratory insufficiency; monitor neuromuscular recovery; alternative to obidoxime
Benzodiazepine	❖ Diazepam: 5–10 mg i.v. slowly, repeat every 10–15 min until seizure cessation ❖ Midazolam: 2–5 mg i.v., or continuous infusion 0.1–0.3 mg/kg/h	Neuroprotection; control of seizures, agitation or CNS involvement; monitor for respiratory depression—ensure readiness for mechanical ventilation

Atropine

Atropine addresses muscarinic symptoms, including bronchorrhoea, bronchospasm and bradycardia.

The dose of atropine is determined by the severity of intoxication, with a maximum daily dose of 50 mg. ²¹ In the present case, treatment with atropine was initiated with a starting dose of 2 mg, which was doubled every 5 min, resulting in a total administered dose of 15 mg. This was followed by continued therapy with a continuous atropine infusion at a rate of 0.05 mg/kg/h until the sixth day of treatment. Although high doses of atropine may not completely abolish cholinergic symptoms, they improve myocardial oxygen utilization and induce marked inhibition of the parasympathetic nervous system. ²² To minimize the risk of atropine toxicity, serum atropine concentrations were closely monitored. Earlier reports have suggested that the therapeutic atropine dose approaches toxic levels and that prolonged use should be avoided because of parasympatholytic effects. However, dynamic monitoring of toxin, cholinesterase, atropine and parasympathetic activity parameters allows precise dose adjustment, thereby preventing atropine toxicity while optimizing therapeutic efficacy.

Obidoxime

In severe poisonings—such as in the present case—atropine monotherapy may be insufficient to achieve clinical improvement, as it merely antagonizes muscarinic effects while leaving the underlying AChE inhibition untreated. Therefore, adjunctive therapy with oximes (obidoxime or pralidoxime) is considered essential. Obidoxime dissociates the bond between organophosphates and acetylcholinesterase, reactivating the enzyme.^35,36 The recommended regimen consists of an initial 250 mg dose, followed by a continuous infusion of 750 mg over 24 h; in selected cases, the infusion may be prolonged for up to 1 week. ³⁷ Obidoxime is most effective when administered as early as possible after exposure, as its reactivation capability declines over time with progressive ‘aging’ of the phosphorylated acetylcholinesterase complex. However, there is no universally applicable time window; the duration of effective therapy depends on the specific organophosphate, its rate of aging and its tissue redistribution. Unlike atropine, obidoxime should not be titrated to clinical effects, as overdosing may worsen toxicity. Consultation with a poison control centre is advised. ²¹

Management of seizures and neurotoxicity

The benzodiazepines employed—most notably midazolam and diazepam—have demonstrated efficacy in the prevention and management of seizures resulting from central nervous system overstimulation. ³⁵ Morphine and related opioids, as well as neuroleptics, should be avoided due to increased seizure risk.

Fluid management and hemodialysis

Studies suggest that adjunctive sodium bicarbonate therapy may enhance the effectiveness of atropine and obidoxime.^38,39 Forced diuresis is ineffective and potentially harmful. ²¹

The role of hemodialysis in Dichlorvos poisoning is limited due to the compound's lipophilicity and large volume of distribution. However, in cases of refractory metabolic acidosis, dialysis may serve as a continuous buffering method. According to the American Heart Association, hemodialysis is recommended only when significant toxin removal is expected or severe acidosis persists despite standard measures. ⁴⁰

Limitations

The study is limited by the absence of quantitative dichlorvos measurements in plasma and urine, as well as by the lack of long-term post-discharge follow-up. Nevertheless, the documented enzyme inhibition pattern and the observed clinical course strongly support the diagnosis and provide meaningful insights for therapeutic decision-making in atypical organophosphate poisoning.

Conclusion

This case of dichlorvos (organophosphate) poisoning showed profound cholinesterase inhibition with paradoxical tachycardia, likely driven by concomitant stimulant exposure (e.g. amphetamines), resulting in an atypical presentation. The resulting sympathetic activation may have contributed to haemodynamic stability and, possibly, to survival. Given that dichlorvos and other organophosphates remain important causes of suicidal self-poisoning, the case illustrates how co-exposures (e.g. amphetamines) can mask classic cholinergic signs and underscores the value of comprehensive toxicology screening and serial erythrocyte/plasma cholinesterase measurements. Effective management hinges on early critical care, guideline-based antidotes (atropine and oximes) titrated to effect and meticulous supportive measures. Severe organophosphate poisoning can present without classical features; clinicians should maintain a high index of suspicion and monitor response to therapy dynamically.